Hello everyone, and welcome to the 2026 JPMorgan Healthcare Conference. My name is Ben Davis. I'm an associate with the JPMorgan Healthcare Investment Banking team, and today I will be introducing Thijs Spoor, Joel Sendek, and Markus Puhlmann, the Perspective Therapeutics team, and they'll be running through the presentation. Afterwards, we'll have a bit of time for Q&A. We'll be passing around the mic for anyone who has questions. Thank you.
Great. Thanks, Ben, and thank you to JPMorgan for inviting us to present at the conference today. My name is Thijs Spoor, the CEO. I do acknowledge that everything that we put out there is current on the SEC website. We may make some forward-looking statements, but we encourage you to look with everything as filed, so I want to tell you first about why I'm in the business, and why I like what we do, and why I'm really passionate, and it always starts and should end with a patient and what happens to a patient, so this woman is in her 80s. She had neuroendocrine cancer, so she had these tumors. She was stable on some atorvastatin for a while, but she had then started to progress, and all these red circles here were tumors that showed up in this woman's abdomen.
And so she needed some kind of interventional treatment. And so a woman in her 80s with a tumor, with multiple tumors, that couldn't just be treated directly. And so we actually treated her with one of our medicines, the VMT-α-NET. And after the first dose of our drug, we were able to see actually a meaningful reduction in those tumors. And if we went further and after four doses of the drug, we actually saw that basically everything shrunk away. The only thing that remained was actually a lymph node that technically stayed and still exists as a lymph node. If that actually had shrunk down, she almost would have considered a complete response, so the ability to actually transform these patients' lives gives us enormous gratitude and gratification for what we're trying to do. We think changing patients' lives is the best thing possible.
And so it's always nice to see real evidence of us directly impacting a patient. So the question is, why radiotherapy? Why Perspective Therapeutics? And really, what does this do in oncology? And over the history of cancer treatment, radiation, the immune system, and chemo have always been really the pillars. How do we actually treat patients with cancer? Cancer is a tough opponent. We want to throw everything we can at it. External beam radiations have been very compelling. But to the degree we can actually bring that radiation inside the patient and treat the cancer from the inside out, we can really transform things. Previously undruggable targets, where they existed on a cancer cell surface but didn't do anything, and therefore were really tough to treat with chemo, are actually really interesting targets for radiopharmaceuticals.
If something shows up on a tumor cell but nowhere else, then we can target it. If we can target it, we can then cause a lot of damage there, and the great thing is it's a validated modality. It's becoming a mainstay. There's growth in the business. What we do is actually having a platform approach to this. These technologies link together. We use a proprietary chemical chelator that actually has been designed for superiority in biodistribution, and so we optimize our medicines to have the best possible biodistribution. We deliver a really potent alpha particle payload. Betas and alphas are fundamentally different from each other. You need about 1,500 betas to kill a cancer cell. A single alpha particle can kill a cancer cell.
And so if you can bring a really highly potent payload, couple it with the right kind of chemistry, and then lever commercial manufacturing capacity, you actually have the amazing ability to transform most patients' lives. And we're actually investing across all three of these to make sure we really bring a lot of value to where we're going. We have three programs in clinic right now. We have a lot of programs that are earlier on. But the neuroendocrine tumor group of tumors we're addressing with VMT-α-NET, we think has the potential for a best-in-class profile. We've designed our medicines to actually show highest possible tumor uptake and lowest possible non-tumor uptake because everywhere the drug goes, we're going to cause damage. We do expect more data updates over the course of this year and throughout 2026.
As we've accepted the various medical meetings, we expect to give updates across the program. I'll dive down a little further on these as we go. We have a melanoma program that we're actively enrolling as well. The really interesting thing about this program is that there's a strong rationale to combine with a checkpoint inhibitor and use combination to really help multiple parts of the body's immune system and the medicines together work to address the tumor. We expect to have some data on that this year as well. Then advanced solid tumors of almost any nature, if physical solid tumors get large enough, they tend to express something. They tend to show stroma, express something called FAP-α, which we can target. Right now, we've got some really interesting data in that program that we expect to talk about this year as well.
Clinically, quite a few catalysts this year, and we also have a strong pipeline behind that. But to explain what makes this feel different and what makes us different. And so we have a proprietary platform. There are three parts of any radiopharmaceutical to think about. One is the isotope that you're choosing to bring your payload. So what you're delivering can either be a gamma ray, a beta particle, or an alpha particle. If you're going to do that with a metal, you have to find some way to drag it to the tumor. And you do that inside a chelator. And chelators are chemical cages. They form a very safe way to bring that metal exactly where you want to attach it. And that chelator, we attach to targeting peptide. You have multiple choices in radiopharmaceuticals. You can use dense proteins. You can use peptides.
You can use antibodies. We actually really like peptides for all the work that we've done, especially in combination with the isotope we've chosen, lead-212. Lead-212 is a fairly short-duration emitter. It's about a 10-hour half-life of the lead-212, and the trade-off there or the benefit there is that if we can get it clearing from the blood very rapidly, we can bring an intense payload to the cell immediately, wait one day, and then the radiation dissipates from the patient, and their body can heal and do much better. One of the things that we are relentless about is actually getting optimized biodistribution, and so having this proprietary chelator will change the charge of the molecule, change the distribution.
And we spend a lot of time behind the scenes making sure we can optimize how the medicine goes to the tumor, and then after that, how we optimize that it doesn't go other places where it's not wanted. And I'll show you some examples of that. So if we have the ability to give potentially superior efficacy and safety, we're going to do our best to make sure we can bring out best-in-class or first-in-class molecules. The chelator itself holds the lead in place, but it also holds the daughter payload. And so lead itself decays to bismuth, and then bismuth gives off an alpha particle. And so you really have to make sure however you're binding your metal, you're thinking about all the downstream as well. These daughter isotopes are almost conceptually like metabolites.
It's not just what happens first, but what happens next to eventually get to something that the body knows how to ignore. After the lead-bismuth decay, you end up with a non-radioactive element that's in picomolar levels. Tiny amounts of mass give extraordinary benefits to these patients. We've also designed this chelator with a net-zero charge. With a peptide drug delivery system, if you have a charged protein, the kidneys will pick up the medicine more so than if it's not charged. By designing it with a neutral charge and to hold the daughter isotope in place, we think we've got a fantastic lead-specific chelator that really helps increase tumor uptake. All this drives therapeutic window. We all know if you give too much of anything, you can actually cause side effects and safety issues.
And you want to give enough that you get a benefit. And that therapeutic window can be incredibly narrow with some medicines, but we're trying to broaden it out as much as we can. And doing that, we can actually then hopefully improve liver and kidney potential side effects. We're often asked the question, which is, what is the best isotope? And the answer is, well, it really just depends. It depends on what you're trying to do. It depends on what you're conjugating to target the tumor. There's trade-offs. And I think about the history of how radiotherapies were delivered. Back in the 1940s, the very first radioactive iodine therapy was given for a patient with thyroid cancer. And radioactive iodine is great for thyroid cancer. It's tricky to incorporate into other biological molecules. It had a lot of chance for off-target.
And so lutetium-177 is now selling in the billions of dollars in medicines made by Novartis. And lutetium worked well because you could chelate it. You could attach it to a peptide and then bring it to a tumor to bring its payload. But the betas have a fairly large zone of damage, about 200 cells. And so there are some trade-offs there for off-target, sort of damage that can happen. The half-life is a trade-off. There is no true theranostic pair. I'll explain that one in a second, which is really how do you identify if the patient has the receptors that you're targeting? And how do you know your medicine can be perfectly calibrated to the patient and understand what goes where? So to increase the potency for lutetium, the scientific community said, let's try actinium. Very similar half-life, almost identical chemistry.
So it meant there weren't a lot of learnings to actually figure out how you actually combine the lutetium or the actinium into a molecule. You got a much higher payload with the alpha emitter. But there's trade-offs because actinium has actually got four active daughters. And those daughters each have their own biochemistry, different charges, different biochemistry. And so you have this issue of other higher risk of off-target toxicity. And so the actinium gave us alpha on the tumor. The francium coming off of that has a different charge and can't be chelated. And so you have this chance of sort of errant daughters throughout the body giving off-target toxicity. Company founders looked at lead and thought, this is fantastic. lead-203, you can image. lead-212 has a therapy. It gives a better anti-tumor activity than the beta because it's so much more potent.
We think by limiting its chance to shine into other organs if you target it, it gives a very good safety profile. It has a very clean, fast decay path, which is good. The half-life means that you're trying to hit the Goldilocks. Not too long a half-life that is causing a lot of extra damage, but not so short you can't actually distribute it and get it to the patient. And what's great is that by having a 10-hour half-life, that's much longer than something like FDG. FDG, used for PET scans, 3.5 million across the U.S., has a two-hour half-life. So we have the luxury of a 10-hour half-life that allows us to actually bring the medicine to patients across the U.S. right now. It's very convenient.
A patient doesn't have to be sequestered from their family for too long if they get this therapy because the radiation disappears so quickly. But what's really exciting scientifically is that there's an elemental twin, lead-203, which we could actually use to then image the tumors and receptors in advance. So lead-203 and lead-212, they're elemental twins. They have identical chemistry, which means for the same composite of matter, you can then get identical biodistribution. And so the analogy is like if you, in advance of taking a test, if you could not only see the questions but the answers, you should do a lot better. And that's what's so exciting for us of how we use this as a patient selection tool. So what we're showing examples here, this poor patient has an osteosarcoma in their shoulder.
And using the lead-203 image, we know that where will the radiation accumulate? Where will it give its damage? In this case, we can see that the bulk of the activity is going to go to the patient's shoulder, cause damage to the shoulder. So before we've given that potent lead-212 alpha emitter, we've just taken the image. Non-invasively, the patient gets a 2 mL injection. They lie under the nuclear medicine camera for 30 minutes. And you can see, do they even have a chance of the therapy benefiting them? And so if you have the chance to actually tell yourself in advance, I know that I'm going to get a really good dose to the tumor and not to other organs, you're in a great position.
And so from the scan, you can see the drug, for the most part, is going to the tumor, or whatever doesn't get bound gets dumped into the bladder, and the patient voids it. And the bladder is actually a very alpha particle-resistant organ. The surface of the bladder sloughs off regularly. And so we actually, it's a safe place for the medicine to go. This means we know where the medicine will target. We can calculate using dosimetry what kind of dose, lifetime dose the patients could get to their kidneys. We can calculate the dose to other organs, to bone marrow, to lung, to brain, to any organ we want. But know in advance that this is going to give a very, very good chance for the patient to be able to knock out this particular target.
When we actually design the medicines, this is something Perspective Therapeutics we think does better than most. And we spend a lot of energy really making sure we get it right. So I'm showing you three mouse images here. And this is showing our work. And so we actually started off with a compound 330 on the far left. And that drug, it went to the mouse as a tumor in its shoulder. You can see that large tumor activity, but just as importantly, you can see an awful lot of activity in the kidney and the bladder. And so there's this very, very strong kidney activity, and you see some bladder. High affinity to FAP-α into the stroma, but also a lot of off-target activity. So these three compounds here have almost identical binding affinity to the FAP-α.
But we then tune the molecule to actually limit the off-target uptake. So the middle image, you see tumor, and you see the kidneys much fainter. And on the far right, you see tumor, and you don't see kidneys. And so it's almost a rhetorical question. Would you rather give a patient the one on the far left that has a high chance of burning the kidneys or the one on the far right that should have a lot less dose and spare them? And it feels obvious when we say it that way, but we encourage anyone looking in the field, anyone innovating in the field, follow the images. It's so important to see the dosimetry, to see the uptake, and to predict in advance where's the medicine going to go. We're really excited about this. The company was a spinoff from the University of Iowa 10 years ago.
We have a fantastic team of chemists that iterates in real time. We can do all this testing in animals without sacrificing them. We can image animals several days in a row, compare compounds within the same model, and not just the same model of animal, but literally the same organism, and see exactly what the difference is between everything, and optimize for tumor, and then optimize to lower tumor and kidney. So are solid tumors an attractive market for radiopharms? Absolutely. We've got Pluvicto that's in the billions of dollars in revenues right now from Novartis. They also have a Lutathera business that's doing incredibly well. Last reported figures that we could tell were at least north of $800 million.
But there are many, many other solid tumor types that create these fantastic total addressable markets in oncology to allow radiopharmaceuticals to kick in and actually do their job and have one more way to target the tumor. Chemo is fantastic. Immunotherapy is fantastic. Radiation adds a third pillar. And if you can deliver that, treat the cancer from the inside out with radiation, we think that's a big boost. One of the obvious questions we often get is, well, it's great if you have the therapy, but you can't make it. We actually have secured with Perspective Therapeutics end-to-end manufacturing. We have our clinical supply secured for a lot of our precursors and isotopes. We are scaling up for commercial. We have sites that are commercially ready, and we have other sites that we're building that are also going to be commercially ready.
We can stockpile one of our parent isotopes that we've been doing, and we have the ability to manufacture all the doses ourselves, so we make the doses at our manufacturing sites, and they get delivered just in time to the hospitals, and we deliver doses right now across many, many states and hospitals regularly in our clinical program, and we need to get the dose to a patient same day. For example, the medicine may leave our facility at 6:00 A.M., and we need to make sure it gets to the patient by 2:00 P.M. If we do that, then we know we actually have a very, very potent thing we can deliver across a scalable network. I think one of the earlier preconceptions was that you could cover the entire country from one facility, and you can.
But what anyone in the isotope business learns very quickly is that you need a network. And if you have a network, you can then supply almost any isotope combination. We've got a fantastic diverse portfolio. In clinic, we have our VMT-α-NET program, which targets SSTR2. We have a melanoma program targeting MC1R. Our PSV359 program targets FAP-α. We've got quite a few programs after that. And we'll update the investment community and the general public once we get first-in-human images. And so we have multiple programs that we're looking after. We want things that have a target that shows up on the tumor and nowhere else. And if we can see it only on tumor, that's a great target for us. As we get first-in-human images, we'll be able to communicate all the other advances we're making. We focus on the lead program for a minute.
So, SSTR2-positive tumors. The bulk of those are neuroendocrine tumors. That's a large market with growing unmet need. There are other tumors that also express SSTR2. It is expressed in small cell lung, breast cancer, meningioma, head and neck. And basically, if you express the target, you can then attach radiopharm to the target and cause damage and destroy it. So Lutathera has been growing quite steadily. There's 170,000 patients living with this disease. And really, they tend to be managed initially for symptomatic relief. But at some point, the patients start to progress. And once they start progressing, you need another therapy. And the first-in-line radiopharmaceutical therapy, we're actually evaluating our medicine to be that first-in-line. One of the things that is a desperate need for patients out there is improved safety and durability for standard of care.
And so what we're trying to really do is say, how can we get patients to live longer lives with higher quality, with better safety? It sounds obvious, but it's really important to demonstrate what this looks like. So our initial phase one data looked fantastic. In patients, if they had any kind of SSTR2 expressing tumor, we had a 39% overall response rate and growing right now. If we just looked at those patients where all their tumors were expressing, we've had a 44% overall response rate and growing. And 78% of the patients so far remained progression-free with greater than one-year follow-up. We haven't hit a PFS number yet because the patients are doing very, very well. And the drug is incredibly well tolerated. We did receive a fast-track designation.
We had initially thought to go in maybe as a post-Lutathera initiative, but the FDA in conjunction with us really was encouraging us to go into the as an alternative in that front-line therapy after the patients have finished a somatostatin sort of tolerance and stability. We're in dose escalation right now, and so we had cohort one. We dosed a few patients there at 2.5 millicuries. The safety was so clear, we moved very, very rapidly, and now we've dosed 46 patients at that cohort two. We've also dosed eight patients at cohort three in the first tranche, and we're adding a few more patients to that group as well. We've actually shown some initial data on those 46 patients, and so the first half of that group, first 23 patients, this was data we showed at ESMO in October this year.
Three months later at ASCO GI last week, we actually showed that all those patients that had received their therapy a year ago, they got four doses eight weeks apart, and then no other therapy from us or anyone else, and we saw the responses deepen, and so having this overall response rate change, 44% response rate, 81% progression-free and alive is absolutely fantastic, and actually, to get a deepening response, these neuroendocrine tumors are slow growing. They're also slow dying, and so as they continue to shrink, we continue to get responses, and the patients actually feel great, and we feel good making sure we can do things that benefit patients. The approval endpoint, though, is not overall response rate. The approval endpoint is progression-free survival or disease control. That's the clinical need. The patients felt great. They were managed on somatostatin analog. They started to progress.
And the first thing the physicians want to do is bring them back to not progressing anymore. And you see with all these ongoing arrows here that at the end of the day, the patients are benefiting. And the majority of these patients remain on study. As we do regular data updates, we'll be able to show all patients with a longer period of time and longer follow-up. If we look at the spider plots, this is looking at every single patient, what's happening with their tumors. We see that the trends are down and to the right. The tumors keep shrinking over time. And if you look at that light blue bar on the left-hand side of the graph, that's when the patients were on therapy, receiving one dose every eight weeks. And then we get into a follow-up period.
If we look at that, you can see that the tumors continue to show shrinkage or they remain stable. That feels great that we can do that to really control the disease in these patients. We just focused on the most recent scan. You can see exactly how we're tracking things through. Not all responses may have been seen. It looks like some of these lines are still sloping down. So at regular updates, we'll be able to communicate what's happening here. When it comes to safety profile, we truly think we have a best-in-class safety profile. So if we look at all the common AEs, we're showing everything here. We had no DLTs, no discontinuations due to adverse events.
The data that we've shown at ESMO and ASCO GI has shown no dysphagia, no serious renal complications, and only modest serious adverse events, none of which was related to the study medication. So these are patients with tumor with no serious adverse events and actually a very, very compelling safety profile. And in comparison to other programs out there, across the board, it appears like we have less side effect profile than comparators. One thing of note, we have not seen major dysphagia that has been seen in other treatments with either the standard of care, Lutathera, or some of the other investigational compounds. We have not seen that yet. We also have not seen any serious renal complications yet as of the latest data cutoffs. So we feel very comfortable we're developing a safe and effective medicine. What should the investment community expect? It's data updates.
And so over the rest of this year, as we get accepted to a medical conference, we'd like to present the data there. We'll be doing updates of that 5 millicuries cohort dose. We also got approval from the FDA to go higher still to 6 millicuries. And we're assessing those patients too. If we increase the dose, do we get more efficacy, earlier efficacy? Do we get more safety signals? We really want to learn and follow the data. But all in a sense, this 5 millicuries dose feels like something that we would like to talk to the regulators about putting into a registrational trial. We feel like we're doing the right thing for patients by having a very good response, by having disease control, and by doing that in a way that appears to be very safe.
Changing gears to another program in our pipeline, we're looking at melanoma patients. 50% of melanoma patients with metastatic disease express something called MC1R. That means 50% do not, and so what we're trying to do is say, if a patient expresses it, how do we pick out which patient could be appropriate and which patient should not be, and the answer is by using the drug itself as an imaging scan, so here you see this poor patient. You see they have a lot of tumors. We can pick up brain mets in this patient, and we see all these tumors that express. If they express, then they can be eligible to go into our study, and we need to really figure out how do we actually extend the reach of checkpoint inhibitors. We do see treatment resistance in these patients.
We do want to make sure that we can actually go with a very precise approach to expand the number of responders and reduce toxicity. The nice thing too about this mechanism of action with an alpha particle smashing into a cancer cell is this should actually help what's going with the immune response. If you can create a new antigenic storm in advance of a checkpoint inhibitor in a patient, you have a higher probability that the immune system will know what to do and should be able to work better in the patient. So we've proven this many times in the mouse model. Now we're assessing this in a very safe fashion to evaluate can this work in patients. Clearly, melanoma is a disease with very high unmet medical needs. The MC1R expression is critical as a selection tool, and we're evaluating both mono and combination approaches.
We're looking at nivolumab and seeing how that works with our medicine, and we're ongoing in a 3- millicurie dose in both monotherapy and combination therapy, so these are patients in the post-second-line plus setting, so anything that we can think of, these patients have seen, and now the disease is progressing, and so in that case, we're able to assess them in either one of two groups. One is a monotherapy, and the other is in a combination, and we do expect to comment about this later this year. The initial results from that study were very interesting, so the patients with the purple line, we think these patients, based on their profile, they all look very similar between the purple and the blue cohorts. The expected PFS in those patients was two to five months. Yet all three patients at the 3- millicurie level went well past that.
Those patients were actually stable disease. It's almost like the disease was frozen in time, which for a melanoma physician treating their patient, it's fantastic. The disease not progressing rapidly is absolutely wonderful. We didn't see a safety issue at the five millicuries level, but we saw that we weren't getting the same level of disease control. And so we've been actually doing our dose ranging and dose finding around that 3 millicuries dose and tracking that forward. So far, we have not seen any major AEs that give us cause for concern. And we saw prolonged PFS with that 3- millicuries dose level. And so the current dose escalation in monotherapy and combination, we expect to have additional reports out on that this year. And our third program targets FAP-α. This is almost like a pan-tumor agent. What does that mean?
The literature has shown so many cases of tumors, solid tumors. When they get large enough, they do one of two things. They have angiogenic behavior, and so they'll form new blood vessel growth to support their own growth, their own vasculature, but they'll also create their own scaffolding and they'll form a stroma, and so the ability actually for the tumor to help itself against the body creates what was previously an undruggable target. The stroma didn't really do much. It protects the tumor, but it wasn't something that chemo could really target directly or have any impact on, but what's so exciting about the radiopharmaceutical field is that if that receptor shows up, if it exists on the cell, then we can target it and cause damage, and that really opens up, we think, a whole range across multiple, multiple indications.
And that should be synergistic with standards of care. If we can reshape the tumor environment, if we can actually get into a massive total addressable market, meaning any solid tumor where the tumors grow large enough to form their own stroma, that's a really good opportunity to change patient care. And how do we tell if the patients actually have it or not? We can image them. We image the patient with the drug itself. And if they're positive, that first patient you saw with the osteosarcoma in their shoulder, great example where we can picture the target we're going after. There's a very clear scientific rationale for going after this. We know this is expressed on cancer-associated fibroblasts. We know that cancer-associated fibroblasts are not good for the patient. We want to make sure we can damage things.
The clinical profile looks strong, and we have a completely novel structure, so this is a composition of matter that has never before been seen in humans. It's not even derived off of anything similar, and so we've designed the medicine to go into the tumor and stay there over time. How long does it stay there? At least two half-lives, and by designing it to go in very, very rapid tumor accumulation, which we can prove with the imaging, and then staying there over at least a day and two days, which is how long the energy gets deposited, we have the plan to really deliver a lot of energy to a lot of different kinds of tumor types. We dose patients at 2.5 millicuries. We went through very quickly and escalated to the 5- millicurie level.
And we're now enrolling in this group, and we're adding then and following data as it goes forward. So with that high tumor retention, with the ability to do that sort of visualization of potential dosimetry by seeing that if we inject a patient within the first hour, we can get the medicine to go very quickly to the tumor or get dumped out of the body and stay there over two half-lives. About 80% of all decays happen within the first day. And that means that we can actually then show something with a high potential to address the tumor microenvironment and to damage the stroma. We innovate constantly. And so we actually have IP that covers composition of matter on everything that we do. We also have IP around the chelator that's proprietary to how we hold the lead in place.
We have a lot of IP around the processes. How do you scale up at commercial level from both the thorium to radium decay, the radium to lead decay, all upstream things that most people never worry about, but are really interesting in this field because we can do this in a very efficient fashion in a way that we've protected? It's also important to look at methods of imaging and treating, and so we keep creating more and more moats to make sure that we have a very, very strong protection of what our scientists do, which they do very, very well. From our last quarterly filing, we had $174 million in cash. We said this will last us to the end of the year. Very strong financial position, fantastic team of people executing on things.
As we look for data catalysts over the year, it looks like we'll have mid-2026 updates on our VMT-α-NET program, on our melanoma program. And later in the year, we'll do updates on our FAP-α as well. And so we're pretty excited about how we're actually developing, bringing these therapies forward. At the end of the day, we have a patient. And the patients in front of us that we see, we can scan them. We can see what this means to them. We can have a meaningful, immediate intervention in their disease. And what's so important about doing a diagnostic scan, if you can get a scan and tell a patient you are suitable or not suitable for the next therapy, that's transformational. And it's so gratifying for us to see these patients actually change their lives.
If we can do it for this patient, we'd like to do it for all patients. Thank you very much.
So to start off the Q&A, what do you think investors are missing about the story?
Thanks, Ben. So I think what's harder for investors to understand is that we are not just a discovery company. We're not just a clinical company. We're not just an isotope production company. Out of necessity, we vertically integrated. And so we do all these things very, very well because we've had to. We would have wanted to, for example, just buy the isotope and label it or find a CDMO. But we realized that we could do most of these things better ourselves as we think about future commercial scalability.
You mentioned the recent data update given at ASCO GI for VMT-α-NET. What's been the initial feedback from clinicians?
So we've actually had fantastic feedback from clinicians. It's great when we have a poster presentation and the physicians come over seeking us, trying to talk to us about the data. But more importantly than that, people saying to us, "We really want to get involved in your study." And so it's not that we want to have competitive enrollment or any of these sort of metrics there. But when clinicians say they're seeking out this medication as an option for their patients, that feels good. And what that tells us is that the data we're showing, we disclose to all the clinicians what we see, what the patients are feeling. And as a result of that, we can then go and talk to physicians about potentially being included in our sites for the current studies or potentially for registrational trial.
You also alluded to the rapid progress you've made so far going from starting human dosing for VMT-α-NET about two years ago to now thinking about a registrational study. What would you say accounts for the speed of the progress you've been able to make?
So I think the patient community in neuroendocrine tumors is very, very well educated. And there's a lot of awareness of compassionate use using a variety of alpha emitters around the world in different jurisdictions. And that's led physicians and patients to think that maybe there's a potential for an alpha therapy to be more potent than a beta. Betas have been very effective at disease control, but there's this quest to do better. Can you lower the overall response rate? Can you get longer disease control? Can you actually have the patients feel better? The initial response that we got from at the North American Neuroendocrine Tumor Society a year and a half ago, we showed some data. And as a result of that, because the patients felt great, they told their doctors they felt great.
The doctor said, "We want more patients to have the ability to have access to this medicine." And so it's been the ripple through to the medical community and the patient community that alphas have a phenomenal potential. And what we're delivering can be done very safely has really driven interest from doctors to include patients in their trials. So we keep adding more sites into our clinical trial program with the hopes that if we get a clearance to do a registrational trial, then we'll be able to go very, very quickly from an operational basis.
So I know you said you had a stockpile of the parent isotope for clinical trials. I was just wondering if you could comment on kind of the supply of the parent isotope if you scale up to kind of a commercial biotech or if you'll have the same issues that actinium's had.
That's a great question. So initially, I studied as a nuclear pharmacist. I worked for Amersham, which is one of the leaders in isotope production. I remember one of my senior mentors saying, "The easiest, cheapest, safest way to make any isotope is to do nothing. Natural decay." So if you can backtrack into what you're looking for, can you get the right precursor? So lead-212 has several parents in the decay chain. But there's one radium-224 that's very interesting. That's what we ship to our production sites. Go back from there to thorium-228 is one that actually has a two-year half-life. That's something you can truly stockpile. We have several years' worth of material on hand in our control. The U.S. Department of Energy has been a fantastic partner. They know how to actually make discrete batches of thorium-228.
We have found in at least six other jurisdictions around the world people who can make thorium-228 as well. And so it's one of the few cases where lutetium, copper, actinium, these isotopes all need on-demand production. And once the isotope has been made, there's a window at which point its purity stays clean enough to actually synthesize into medicine. But after that, you need something new. And so that's a very tight supply chain. We have the luxury of having upstream things we can stockpile and store. So if, for example, every single thorium-228 production site in the world shut down now, we would still be fine for several years. The nice thing is that we replenish our pool of thorium-228 as needed. And it's been great to work with the U.S. Department of Energy to do this.
They used to have thorium-228 as a waste byproduct from another material they made. Now they've actually figured out how to make it specifically for this industry. And they've leaned in and done what they can to help out the medical industry.
Now that you've started to have a bit of clinical data from VMT-α-NET, how has the data so far evolved relative to your expectations based on how the construct was designed?
So when we first thought about the medicine, I mean, the company was a spin-out at the University of Iowa and came with inspiration for the Pediatric Neuroendocrine Center of Excellence. We thought, can we design a medicine that's going to be safer and more effective for kids? And by doing that, by having it tuned so it was designed to go more to the tumor and less to the kidney, the hypothesis was also that this could be safer for adults as well. And that thesis has played out. We've done the animal biodistribution work. We've shown imaging in animals. We've treated animals. We've done imaging in humans. And when all that data came together, we said, "Great.
This is an important medicine to go forward and actually use to treat humans with," so if I talk to the scientific founders, they'll say, "We knew it all along," and they have great confidence, and that's fantastic. We all know that mouse data doesn't always translate to human data, but what's really exciting now is that it really looks like, in this case, it does. We are getting fantastic responses.
What do you think would drive broader use of radiopharmaceuticals as oncology therapeutics?
I think that the meaningful patient benefit is driving an adoption here. There have been some issues around the industry of trying to identify enough trained clinicians that can administer the pharmaceuticals, enough trained administration suites that can deliver product. Novartis has done a very good job of actually educating the patient community. The reimbursement is in place. There are more and more techniques coming in to look at dosimetry. There's more and more techniques to figure out how you can actually do patient management better, patient throughput better. But I think the growth of clinical data showing you can have a meaningful change in patient outcome if you can screen them first and then treat them with a targeted therapy. My understanding from last count is there are at least 80 companies developing new medicines in the radiopharmaceutical space.
Not every medicine will make it, but an awful lot should.
You had touched on this. But given the half-life of lead-212, how do you view the supply chain infrastructure needed to bring these therapies to patients at scale?
So each jurisdiction needs its own supply chain in this case. You can almost think of it as like fresh baked goods. These aren't going to store on the shelf for weeks at a time or even days at a time. Rather than think about half-life, we think about shelf life. And the shelf life on agents that we make tend to be more in this sort of same-day kind of shelf life for 24 hours. Some of the other medicines will have a 48-hour shelf life, which gives them a little bit more time, but not too much. The answer to the industry has been build a network. And so we have a facility in New Jersey that produces product just about every day. We have a facility in Iowa that does the same thing. We're building a new site in Chicago.
We've purchased buildings in Houston and LA and also working with looking at either our own sites or CDMO partners in other jurisdictions, so if you have a network, you can actually then do almost any program through it, and we're in the middle of establishing what we think is a very strong, commercially reliable network.
Perfect. Well, I think that's all the time we have for today. Thank you very much to the Perspective Therapeutics team. And thank you all very much for coming.
Thank you.